Cited by 213Sulfur Compounds in BiologyRedox biology and oxidative stressGlutathione Transferases and Polymorphisms

Glutathione in Brain Disorders and Aging

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Iskusnykh, Igor Y., Zakharova, Anastasia A., Pathak, Dhruba·2022·Molecules

Abstract

Glutathione is a remarkably functional molecule with diverse features, which include being an antioxidant, a regulator of DNA synthesis and repair, a protector of thiol groups in proteins, a stabilizer of cell membranes, and a detoxifier of xenobiotics. Glutathione exists in two states—oxidized and reduced. Under normal physiological conditions of cellular homeostasis, glutathione remains primarily in its reduced form. However, many metabolic pathways involve oxidization of glutathione, resulting in an imbalance in cellular homeostasis. Impairment of glutathione function in the brain is linked to loss of neurons during the aging process or as the result of neurological diseases such as Huntington’s disease, Parkinson’s disease, stroke, and Alzheimer’s disease. The exact mechanisms through which glutathione regulates brain metabolism are not well understood. In this review, we will highlight the common signaling cascades that regulate glutathione in neurons and glia, its functions as a neuronal regulator in homeostasis and metabolism, and finally a mechanistic recapitulation of glutathione signaling. Together, these will put glutathione’s role in normal aging and neurological disorders development into perspective.

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  • The reported loss in GSH in given brain areas in some human diseases is likely to be at least in part the consequence of a loss of astrocytic GSH and/or of alterations in the GSH metabolism of astrocytes.

    “As a consequence of the high abundance of astrocytes in the brain and of the well‐known pivotal role of astrocytes in brain GSH metabolism, it can be concluded that the reported loss in GSH in given brain areas in some human diseases (Detcheverry et al. 2024; Iskusnykh et al. 2022) is likely to be at least in part the consequence of a loss of astrocytic GSH and/or of alterations in the GSH”

    From Glutathione Metabolism of the Brain—The Role of Astrocytes (2025) · cites this paper as Iskusnykh et al. 2022

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Authors
Iskusnykh, I. Y., Zakharova, A. A., & Pathak, D.
Affiliations
  • University of Tennessee Health Science Center (US)
  • Pirogov Russian National Research Medical University (RU)
  • Temple University (US)
Corresponding author
  • Iskusnykh, Igor Y.
  • Pathak, Dhruba
Venue
Molecules
Publisher
MDPI AG
Published
2022-01-05
Volume
27
Issue
1
Pages
324
ISSN
1420-3049 (ISSN-L)
OpenAlex
W4206843434
Cited by
213
References
5
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FWCI
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journal article
Language
en
Open access
Locations
  • Molecules (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • TUScholarShare (Temple University) (submittedVersion, cc-by)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glutathione Transferases and Polymorphisms
Keywords
glutathione, brain aging, neurological disorders, oxidative stress, glutathione redox state, antioxidants, DNA repair, thiol protection, xenobiotic detoxification, neuronal homeostasis, glial cells, Huntington's disease, Parkinson's disease, stroke, Alzheimer's disease
MeSH terms
Aging, Animals, Brain, Brain Diseases, Disease Susceptibility, Glutathione, Homeostasis, Humans, Nerve Degeneration, Nervous System, Neuroglia, Neurons, Oxidation-Reduction, Biomarkers, Metabolic Networks and Pathways

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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